Abstract
The intervertebral disc is believed to be the key pathology behind low back pain (LBP). The pain mechanisms include annular ruptures, fissures in the end plates, neural sensors on the disc surface causing muscle stimulation,1 in combination with various biochemical reactions, particular involving cytokines. Disc herniations are not dealt with this review.
The ruptures/fissures in the annulus and end plates may cause pain directly, if annular ruptures reach the disc surface. Beside these classical physical aspects, it is increasingly clear that inflammatory cytokines play a role.2 Also, there are convincing indications that the cytokine TNF-α passes the annular ruptures and irritates the disc surface.3 The newest recognized pathology is that end plate ruptures may give rise to modic changes, possibly caused by low-virulent anaerobic bacteria.
Intradiscal treatments have been used and tested over the years. The theories behind the first such treatments, chymopapain and intra-discal electro-thermal therapy (IDET), was the mechanical issue that the jelly-like and toxic nuclear material may penetrate through the annular ruptures. Probably, Mother Nature has decided that when annular ruptures become a problem, nucleus should be more fibrotic preventing its penetration. If this fibrosing can be accelerated in an early degenerated phase, part of the problem might be reduced. Later years, injection treatments rather consider the biochemical aspects.
Such treatments will briefly be discussed in the article. For them all, the demonstrated likelihood of later developed degeneration is a potential disadvantage for any intradiscal injection.4
None declared
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